Anaphylactic Shock

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ANAPHYLACTIC SHOCK

Bhagya Gunetilleke
Consultant Anaesthetist/ Senior Lecturer
Faculty of Medicine
University of Kelaniya
Learning Outcomes

 Outline the pathophysiology


 Describe the clinical presentation
 Discuss the management of anaphylactic
shock
Anaphylaxis

 Severe, life threatening, generalized or


systemic hypersensitivity reaction
characterized by rapidly developing, life
threatening changes to the
Airway +/- breathing +/- circulation

 1 in 1300 experience anaphylaxis during their


lifetime (UK data)
 Commoner in females
Clinical Scenario - 1

 25 year old male, presented with features of


cellulitis.
 C/O difficulty in breathing, pruritus and
faintishness soon after the first dose of iv Benzyl
penicillin.
 Heart rate 120/min, blood pressure 70/40mmHg

 What is the most likely diagnosis?


 What would you do if you are the House officer?
Pathophysiology-1

 IgE mediated type-1 hypersensitivity reaction


 Previously sensitized to allergen/ antigen
 Generates an immune response, mainly IgE
 Mast cells coated with IgE
 Subsequent exposure to same antigen leads
to binding to IgE & exaggerated response
 Response is not proportional to antigen load
 Histamine, Leukotrienes, Serotonin
Pathophysiology-1
Time To Cardiac Arrest After Exposure
Commonly Identified Triggers

 Food – Peanuts, fish, milk


 Stings -Wasps
 Medicine – Penicillin’s, cephalosporin’s,
suxamethonium, NSAIDs, ACEi, Gelatin
solutions
 Cosmetics – Latex, hair dye
Diagnosis–Cardinal features

 Sudden onset & rapid progression


 Features of compromised Airway +/-
Breathing +/- Circulation
 Skin/ mucous membrane lesions lesion
Pathophysiology & Clinical
features-2
 Sudden onset, Rapid progression following
exposure to an antigen
 Stridor, hoarseness,
Increased capillary permeability,
extravasation & edema e.g.. tongue,
oropharynx, larynx - angioedema
 Rhonchi
Dyspnoea, bronchospasm & secretions,
exhaustion & respiratory arrest
Laryngeal Edema

Normal larynx Edematous larynx


Pathophysiology & Clinical
features-2
 Hypotension & Cardiac arrest
Vasodilation, reduces afterload
Venodilation reduces preload
Myocardial depression

 Confusion – cerebral hypoxia

 Flushing, angioedema, urticaria - Skin/ mucosal


changes alone are not signs of anaphylaxis
Urticaria
Pathophysiology & Clinical
features-3
 Syncope – Cerebral hypoperfusion /
hypotension
 Diarrhea & vomiting – Edema & secretions of
gastrointestinal tract

 Differentiate from
Severe asthma
Septic shock
Cardiac failure
Anaphylactoid Reactions

 Similar clinical picture


 Not a hypersensitivity reaction. Mediated by
complement system (not IgE)
Hence no previous exposure to antigen
 Severity proportional to antigen load (dose)
 Common cause – Radio- contrast media
Management - 1
 Aims
Restore oxygenation & perfusion of brain/ heart
Reverse pathological changes
Prevent repeat exposure
Management - 2

A.B.C.D.E Approach
 Stop further exposure to antigen – Stop
injecting
 Call for help
 High flow O2 via mask
 Assist ventilation /ambu bag
 Prepare for intubation
 Elevate lower limbs – increase venous return
 IV access/ IV crystalloid- What?
High Flow Oxygen
Assisted Ventilation via Ambu bag
Management - 2

 Drug of choice

ADRENALINE
As soon as possible!
Intramuscular (IM) 1:1000 0.5ml doses
Intravenous (IV) 1:10,000 0.5ml doses
Adrenaline – Self injection
Management - 3

 Hydrocortisone 200mg iv – to inhibit


inflammatory response
 H1 receptor antagonist eg, Chlorpheniramine
10mg iv
 H2 receptor antagonist eg Ranitidine 50mg iv
to inhibit further release of Histamine
Management - 4

 Serum tryptase assay


 Educate the patient
 Documentation
 Refer to immunologist

Medic alert bracelet to be worn by patient


Serum Tryptase Assay
Prevention of Complications

 Anticipate
 Drug and allergic history
 Check emergency equipment/ drugs daily
Case scenario - 1

 What is the diagnosis?


 How do you manage the patient?

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